Does tumor necrosis factor α inhibition promote or prevent heart failure in patients with rheumatoid arthritis?

Autor: Anja Strangfeld, Jörn Kekow, Angela Zink, Siegfried Wassenberg, Joachim Listing, Matthias Schneider, Andreas Kapelle
Rok vydání: 2008
Předmět:
Adult
Male
medicine.medical_specialty
Heart disease
Immunology
Antibodies
Monoclonal
Humanized
Severity of Illness Index
Gastroenterology
Receptors
Tumor Necrosis Factor
Etanercept
Arthritis
Rheumatoid
Cohort Studies
Rheumatology
Risk Factors
Germany
Internal medicine
medicine
Humans
Immunology and Allergy
Pharmacology (medical)
Longitudinal Studies
Prospective Studies
Glucocorticoids
Aged
Proportional Hazards Models
Heart Failure
Cyclooxygenase 2 Inhibitors
Tumor Necrosis Factor-alpha
business.industry
Proportional hazards model
Hazard ratio
Adalimumab
Antibodies
Monoclonal
Middle Aged
medicine.disease
Infliximab
Residual risk
Interleukin 1 Receptor Antagonist Protein
Treatment Outcome
Endocrinology
Antirheumatic Agents
Immunoglobulin G
Rheumatoid arthritis
Heart failure
Female
business
medicine.drug
Zdroj: Arthritis & Rheumatism. 58:667-677
ISSN: 1529-0131
0004-3591
DOI: 10.1002/art.23281
Popis: Objective To determine the hazard risk of developing or worsening heart failure in rheumatoid arthritis (RA) patients treated with tumor necrosis factor α (TNFα) inhibitors. Methods RA patients ages 18–75 years who started treatment with infliximab, etanercept, or adalimumab (n = 2,757), or conventional disease-modifying antirheumatic drugs (controls; n = 1,491) at the time of enrollment in a German biologics register were studied. Cox proportional hazards models were applied to investigate the influence of disease-related and treatment-specific risk factors on the incidence or worsening of heart failure. Results The 3-year incidence rates of heart failure in patients with and patients without cardiovascular disease at the start of treatment were 2.2% and 0.4%, respectively. After adjustment for traditional cardiovascular risk factors, an increased risk of developing heart failure was found in patients who had a higher 28-joint Disease Activity Score at followup (hazard ratio [HR] 1.47 [95% confidence interval 1.07–2.02], P = 0.019). A residual nonsignificant risk related to treatment with TNFα inhibitors remained (adjusted HR 1.66 [95% confidence interval 0.67–4.1], P = 0.28). This residual risk was balanced by the efficacy of the anti-TNF treatment. When only baseline characteristics were taken into account, the HR related to TNFα inhibitor treatment decreased to 0.70 (95% confidence interval 0.27–1.84). Conclusion The findings of this study indicate that TNFα inhibitor treatment that effectively reduces the inflammatory activity of RA is more likely to be beneficial than harmful with regard to the risk of heart failure, especially if there is no concomitant therapy with glucocorticoids or cyclooxygenase 2 inhibitors. Furthermore, the data suggest that TNFα inhibition does not increase the risk of worsening of prevalent heart failure.
Databáze: OpenAIRE
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